In the present study, we tested the hypothesis that environmental pollutants are dose-dependently associated with increased risk for alanine aminotransferase elevation and suspected nonalcoholic fatty liver disease in the NHANES adult population.

In our study, we showed that selected relevant air pollutants produce a significant clustering of the Texan counties with respect to their concentration and discussed about the incidence rate distributions of liver cancer over the identified clusters.

No increased risk of mortality and morbidity was found in the entire area among people living close to incinerators. The internal analysis of the cohort based on dispersion modeling found excesses of mortality for some cancer types in the highest exposure categories, especially in women. People in the highest heavy metal exposure categories tended to have a lower socioeconomic status than those in the lowest categories. The interpretation of the findings is limited given the pilot nature of the study

The results support a comparatively high adjusted relative risk of liver injury among patients exposed concurrently to multiple antimicrobials and modest elevations in the risk for several antimicrobials used alone; however, we found little evidence of any strong effect of commonly used antimicrobials on the risk of liver injury.

Taking together our findings in the present study and previous evidence of increased mortality from other causes of death, we conclude that arsenic in Antofagasta drinking water has resulted in the greatest increases in mortality in adults < 50 years of age ever associated with early-life environmental exposure.

We found elevated hazard ratios (with wide confidence intervals) at Camp Lejeune for causes of death from cancers of kidney, liver, esophagus, cervix, multiple myeloma, Hodgkin lymphoma, and amyotrophic lateral sclerosis; however, because less than 6% of cohort had died, long-term follow-up is necessary to comprehensively assess effects of drinking water exposures at the base.

This study found evidence for excess hepatobiliary cancer mortality among workers exposed to vinyl chloride in a chemical manufacturing plant, as well as a trend with 20-year lagged duration of exposure.

We report urinary biomarkers for occupational exposure to N,N-dimethylformamide and reveal dose-response relationships between their levels and liver injury, with males having a greater risk of injury.

The objective of this study was to for the first time perform a cumulative health risk assessment of the 17 perfluoroalkylated and polyfluoroalkylated substances measured in the Swedish population, individually and in combination, using the Hazard Index approach.

Median income by county was inversely associated with chronic liver disease mortality, while the logarithmically transformed airborne concentrations of on-road manganese were positively correlated with county-level chronic liver disease mortality

This suggestion of an association between metolachlor and liver cancer among pesticide applicators is a novel finding and echoes observation of increased liver neoplasms in some animal studies; however, our findings for both liver cancer and follicular cell lymphoma warrant follow-up to better differentiate effects of metolachlor use from other factors.

This study showed lower levels of perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) and slightly higher levels of perfluorohexane sulfonate (PFHxS) than other published population studies. Our results did not give significant evidence to support the association with cholesterol outcomes with PFOS and PFOA. However, we did observe several significant associations with the PFHxS and cholesterol outcomes.

We found no significant positive relationships between serum perfluorooctanoate and liver or renal function tests, cholesterol, thyroid-stimulating hormone, or with red cell indices, white cell, or platelet counts; mean serum perfluorooctanoate was not increased in liver or thyroid diseases.

We calculated the standardized mortality ratio (SMR) for the atomic bomb survivors versus the entire population of Japan in childhood and compared them with a true non-exposed group. A notable result was that SMRs in boys exposed to low doses were significantly higher for solid cancer.